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Published on: May 19, 2020
Association of immune cell recruitment and BPD development
Motaharehsadat Heydarian1, Christian Schulz2,3, Tobias Stoeger1
1Institute for Lung Health and Immunity and Comprehensive Pneumology Center with the CPC-M bioArchive, Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Insights
Bronchopulmonary dysplasia (BPD) arises from neonatal lung injury due to prenatal and postnatal factors. This review examines inflammatory responses and myeloid cell roles, suggesting new therapeutic strategies based on immune system differences.
Area of Science:
- Neonatal medicine
- Pulmonology
- Immunology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in neonates.
- It results from prenatal and postnatal risk factors, including inflammation.
- Immaturity and specific exposures exacerbate lung injury.
Purpose of the Study:
- To review the link between neonatal lung immaturity, exposures, and BPD development.
- To highlight the role of inflammatory responses and myeloid immune cells in BPD.
- To explore therapeutic strategies based on immune system disparities.
Main Methods:
- Literature review focusing on BPD pathogenesis.
- Analysis of inflammatory pathways and immune cell function.
- Comparison of infant and adult immune systems.
Main Results:
- Prenatal/postnatal factors trigger inflammatory networks in the neonatal lung.
- Cytokine release, protease activity, and immune cell infiltration contribute to lung injury.
- Neutrophils and monocyte/macrophages are key myeloid cells in the BPD lung.
Conclusions:
- Inflammatory processes driven by myeloid cells are central to BPD.
- Understanding immune system differences can guide novel BPD therapies.
- Targeting specific inflammatory pathways may offer therapeutic benefits.
Abstract:
In the neonatal lung, exposure to both prenatal and early postnatal risk factors converge into the development of injury and ultimately chronic disease, also known as bronchopulmonary dysplasia (BPD). The focus of many studies has been the characteristic inflammatory responses provoked by these exposures. Here, we review the relationship between immaturity and prenatal conditions, as well as postnatal exposure to mechanical ventilation and oxygen toxicity, with the imbalance of pro- and anti-inflammatory regulatory networks. In these conditions, cytokine release, protease activity, and sustained presence of innate immune cells in the lung result in pathologic processes contributing to lung injury. We highlight the recruitment and function of myeloid innate immune cells, in particular, neutrophils and monocyte/macrophages in the BPD lung in human patients and animal models. We also discuss dissimilarities between the infant and adult immune system as a basis for the development of novel therapeutic strategies.
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